In human central nervous system (CNS), it is very difficult to regenerate the neuronal axon which was once injured due to spinal cord injury, cerebrovascular disease, cerebral injury or the like and, once a deficit symptom of motor function or sensory function happens, recovery therefrom is difficult whereby one shall suffer from the aftereffects thereof throughout his/her life. That has been well known not only among persons skilled in the art but also among common people and, in recent years, the reasons thereof have been gradually clarified. For the recovery of neural function, there is needed the regeneration of neuronal network by an elongation of neuronal axon cut by injury beyond the injured area resulting in synapse formation connected to the secondary neuron. However, the environment surrounding the central nervous system is equipped with a regeneration inhibiting function via plurality of regeneration suppressing factors for neuronal axons for preventing the disordered formation of synapse and this function disturbs the regeneration of neuronal network. Chondroitin sulfate proteoglycan has been known as one of the regeneration suppressing factors for neuronal axon and has been reported to inhibit the axonal regeneration in the injured area (refer, for example, to Non-Patent Literature 1). Further, in Patent Literature 1, the fact that keratan sulfate plays an important role in the formation of glial scar inhibiting the axonal regeneration is clarified by an experiment in brain-injured model using mice where N-acetylglucosamine 6-O-sulfotransferase 1 (GlcNAc6ST-1) gene which is necessary for biosynthesis of keratan sulfate in the brain is knocked out. In the same document, it is proposed that substances which inhibit the synthesis and the physiological activity of keratan sulfate are effective for the prevention and the treatment of nerve damage from the experimental results that non-expression of keratan sulfate in the injured area results in the suppression of the formation of glial scar.
Further, expression of neuropathic pain is exemplified as a symptom which greatly lowers the QOL (quality of life) among sensory neuron dysfunction. Neuropathic pain is a pain caused by disorder of the central nerve or the peripheral nerve and examples thereof include spontaneous pain, hyperalgesic reaction where the threshold for invasive stimulation lowers and mechanical allodynia where non-invasive mechanical stimulation and tactile stimulation which usually do not induce the pain are erroneously recognized as sharp pain. Examples of the diseases expressing neuropathic pain include cerebral disorder, multiple sclerosis and spinal cord injury as central ones and diabetes mellitus and herpes zoster as peripheral ones. Among neuropathic pains, allodynia is characterized in that intractable and burning pain and piercing pain continue for a long period of time without intermittence and is also a cause of the reduction in the effect of rehabilitation due to the pain. There has been almost no satisfactory drug therapy for neuropathic pain and there has been a demand for the development of drugs which satisfy both pharmaceutical effect and safety. However, the development of the drug has been unable to make satisfactory progress. One of the reasons therefor is that it is thought that the mechanism of pathogenesis is not single but many of them are entangled in a complicated manner. Details of the onset mechanism for allodynia is still ambiguous even at this time but, in recent years, findings for ATP (adenosine triphosphate) which has been known as a pain-causing substance have started to be reported. It has been gradually aware of that ATP strongly activates spinal microglia and causes potentiation of production of various mediators assisting the abnormal neuronal network formation, synapse transportation and release of neurotransmitters with re-construction of cell skeleton whereby it participates in neuropathic pain, and ATP as such also activates Rac which is one of an Rho family (Non-Patent Literature 2).
It has been also being aware of that spinal microglia of dorsal horn is activated by nerve injury and that stimulation of P2X4 receptor which is strongly expressed therein causes neuropathic pain, and it has been proposed of the participation of Rho kinase signal transduction system as one of the routes of cascade of the activation as such (Non-Patent Literature 2).    Patent Literature 1: JP-A-2006-290842    Non-Patent Literature 1: Niederost, B. P., Zimmermann, D. R., Schwab, M. E. & Bandtlow, C. E. Bovine CNS myelin contains neurite growth-inhibitory activity associated with chondroitin sulfate proteoglycans. J. Neurosci. 19, 8979-8989 (1999).    Non-Patent Literature 2: Honda, S. et al., 2001. Extracellular ATP or ADP Induce Chemotaxis of Cultured Microglia through Gi/o-Coupled P2Y Receptors. J. Neurosci. 21(6), 1975-1982.